Abstract

PIP: After reviewing the pathophysiology of the menopause, attention is directed to a review of the benefits of estrogen progestogen replacement therapy (vasomotor symptoms, urogenital atrophy, psychosomatic complaints, osteoporosis, cardiovascular disease, lipid metabolism); the risks of estrogen progestogen replacement therapy (endometrial cancer, endometrial hyperlasia, breast cancer, coagulation factors, gallbladder disease); and evaluation for estrogen therapy (nonoral estrogen administration). This author regards the menopause to be a hormonal deficiency state, and, like all endocrinopathies, should be managed as vigorously as need be, and without a necessary limitation of time. A wide variety of physical changes and symptoms have been associated with the climacteric. Some patients may only experience cessation of menses; others experience severe reactions that are occasionally disabling. Several factors may influence development of symptoms during the postmenopausal years, and the most important factor is probably the degree of estrogen depletion and the rate at which estrogen levels decrease. Additional factors may be an inherited or acquired propensity to withstand or succumb to the aging process and the psychologic impact of aging and the woman's ability to accept or deny the emotional changes of the menopause. The proven and almost universally accepted benefits of estrogen replacement therapy include relief of vasomotor symptoms, prevention of atrophic vaginitis, and prevention of osteoporosis. Estrogens may also help alleviate some of the psychogenic manifestations that menopause aggravates. Decreasing the risk of cardiovascular disease, particularly in oophorectomized young women may be another benefit by estrogen increased HDL cholesterol. 10 days of cyclic progestogen reduces the risk of endometrial cancer by preventing or treating estrogen induced endometrial hyperplasia. The risk of breast cancer has not been shown to be increased with estrogen therapy, and progestogens may provide additional protection for this tumor. The prognosis for breast carcinoma developing in hormone users is improved, most likely because of an earlier detection. Estrogens prevent demineralization of bone, and the addition of progestogen apparently promotes new bone formation. An increased risk of gallbladder disease may be associated with estrogen therapy, but this risk is minimal and has not been observed in all studies. There is no evidence that either estrogens or progestogens, in the small doses needed for menopause, increase the risk of thromboembolic disease. Newer routes of estrogen administration may further reduce the risks and increase the benefits.